Disease relevance of Vagistat-1

• After vaginal insertion of a 300-mg ovule of tioconazole in 10 patients with vaginal candidiasis, the mean concentration in plasma was 21.2 ng/ml (range, 10.6 to 35.8 ng/ml) at 8 h and was not measurable at 24 h in 9 of 10 patients [1].
• Preliminary studies in other clinical areas suggest tioconazole may be useful for treating onychomycosis (in a special nail formulation), napkin-rash due to Candida albicans, impetigo, and vaginal trichomoniasis, although comparative studies are needed in each of these settings to clearly assess its relative place in therapy [2].
• Tioconazole. A review of its antimicrobial activity and therapeutic use in superficial mycoses [2].
• Single-dose tioconazole compared with 3-day clotrimazole treatment in vulvovaginal candidiasis [3].
• In contrast to C. albicans, the Gram-positive bacterium, Staphylococcus aureus H, which lacks membrane sterols, showed no trailing endpoints with tioconazole after either shaken or static incubation [4].

High impact information on Vagistat-1

• General equations and data analysis methods are presented to relate mobilities to equilibrium constants in simple and competitive binding equilibria and used to determine thermodynamic parameters for host-guest complexation of tioconazole enantiomers with a range of cyclodextrin selectors [5].
• Thus, tioconazole is an effective and well tolerated treatment for vaginal candidiasis and superficial fungal infections of the skin [2].
• At a concentration of 3.8 X 10(-5) M, tioconazole, like miconazole, caused rapid 2- to 3-log reductions in CFU per milliliter when added to late-logarithmic-phase Candida albicans or Candida parapsilosis cells [6].
• Bioluminescent assays of fungal ATP in cultures of Candida albicans exposed to tioconazole and ketoconazole demonstrated that intracellular ATP levels were directly related to cell viability [7].
• Studies of the kinetics of killing indicated that the drugs studied could kill under conditions used for the MFC determination and that tioconazole and ketoconazole could kill particularly rapidly [8].

Chemical compound and disease context of Vagistat-1

• The anti-inflammatory activities of eight anti-fungal agents (butoconazole, ciclopirox olamine, fluconazole, miconazole nitrate, sertaconazole nitrate, terconazole, tioconazole and ketoconazole) were compared in a number of preclinical models of dermal inflammation and pruritus [9].
• Treatment of dermatomycoses with topical tioconazole and miconazole [10].
• Overall, topical therapy with tioconazole was preferred over systemic ketoconazole therapy for these women with symptomatic vulvovaginitis due to Candida albicans [11].
• At the long-term follow-up evaluation approximately 6 weeks after treatment for patients with diaper rash, the overall cure rate was about the same in both tioconazole- and comparative imidazole-treated patients (87% and 90%, respectively), and 14% in patients using vehicle cream [12].
• Open comparison of the efficacy, toleration and safety of tioconazole cream and econazole ovules used in the 3-day treatment of patients with vaginal candidiasis [13].

Biological context of Vagistat-1

• Serum 17 beta-oestradiol was unaffected, but LH was raised on days 19 and 20 p.i. In animals receiving progesterone (2.5 mg/animal/day, s.c.) and tioconazole from day 18 p.i. parturition was no longer advanced [14].
• In contrast, tioconazole (IC50 range 0.18 to 3.3 microM) and miconazole (IC50 range 0.15 to 10 microM) were relatively non-selective [15].

Associations of Vagistat-1 with other chemical compounds

• Three imidazole antifungal agents, ketoconazole, miconazole and tioconazole, and a group of structurally related 1-substituted imidazole and 1,2,4-triazole compounds were evaluated as inhibitors of the oxidative metabolism of testosterone catalysed by mouse hepatic microsomal cytochromes P-450 [15].
• Two topical antifungals, butoconazole and terconazole, and two systemic antifungals, itraconazole and vibunazole, gave mean RIFs less than 60% in tests with Candida species, and therefore matched clotrimazole, ketoconazole and tioconazole in terms of RIF [16].
• In vitro assays demonstrated that clinical yeasts were significantly more inhibited by tioconazole (MIC50, < or = 0.5 microgram/ml) than by fluconazole (MIC50, 8 micrograms/ml) [17].
• The present study suggests that tioconazole is an important contact allergen, which should be included into the patch test series in countries where it is used as a topical antifungal agent [18].
• Northern blot analyses revealed an increased level of transcription of the TruMDR2 gene when mycelium was exposed to acriflavine, benomyl, ethidium bromide, ketoconazole, chloramphenicol, griseofulvin, fluconazole, imazalil, itraconazole, methotrexate, 4-nitroquinoline N-oxide (4NQO) or tioconazole [19].

Gene context of Vagistat-1

• Effects of tioconazole on parturition and serum levels of 17 beta-oestradiol, progesterone, LH and PRL in the rat [14].
• Development and optimisation of a high-performance liquid chromatographic assay for tioconazole and its potential impurities. Part II. Selection of detection conditions for potential impurities [20].

Analytical, diagnostic and therapeutic context of Vagistat-1

• Capillary electrophoresis with chiral selectors: optimization of separation and determination of thermodynamic parameters for binding of tioconazole enantiomers to cyclodextrins [5].
• Both open and controlled clinical trials have clearly demonstrated the efficacy and safety of topical preparations of tioconazole for treating superficial dermatophyte or yeast infections of the skin and vaginal candidiasis [2].
• Except for the first 6 months, the incidence of positive patch test reactions to tioconazole was over 1% of patients tested for contact allergy [18].
• Two clinical trials were performed to determine the relative efficacy of tioconazole, a new antifungal agent for treating patients with tinea pedis [21].
• In contrast, isolate 1084-S, which was found by pulsed-field gel electrophoresis and random amplification of polymorphic DNA to be genetically closely related to isolate 1084-L, exhibited cross-resistance to the azole compounds except tioconazole [22].

References